In summary, Rg1 exhibits anticerebral ischemia activity that may be attributed to its ability to increase VEGF expression via the PI3K/AKT/mTOR signaling pathway [85], alleviate oxidative stress by inhibiting miR-144 activity and subsequently promoting Nrf2/ARE pathway activity [86], increase BDNF expression and downregulate inflammatory cytokine expression [89], inhibit p38/JNK2 phosphorylation in NSCs [87], and downregulate PAR-1 expression [88]. Here, NFE2L2 is linked to ischemia.